Blood supply to the human femoral diaphysis in youth and senescence.

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The nutrient foramina in the human femoral diaphysis were counted in 109 cleaned and dried bones, ranging in age from 38 to 98 y. Although statistical analysis for univariate associations found that foramen number was not linked to age, sex (male/female) or side (R/L), multivariate logistic analysis revealed a significant interaction between the effects of sex and side (P < 0.01). Univariate analysis for sex and for side separately revealed a significant difference in for men number between the results for men and women for R bones 62% (18/29) vs 33% (8/24) (P < 0.04), but not for L bones 35% (9/26) vs 48% (13/27) (P < 0.28). One lower limb from 15 cadavers was perfused with a barium sulphate suspension to show the blood supply of the femoral diaphysis. Twelve were in the age group 59-88 y and considered to be senescent material. In addition, 3 more femora were perfused, 1 from a young male aged 21 y, another from a 42-y-old male considered to show early senescent changes, and a third from a man aged 56 y with a hip prosthesis in situ, to provide an example of a cortex deprived entirely of its medulla. All perfused femora were fixed and decalcified, and sections were then radiographed. Cross-sections through the middiaphysis showed that aged bone cortex is supplied predominantly from the periosteum in contrast to the medullary supply in young human and animal material. The change is attributed to increasingly severe medullary ischaemia with age, brought on by atherosclerosis of the marrow vessels. An examination of the findings reported by investigators of animal bone blood supply in the past 40 y shows a large measure of agreement. Long standing controversy seems to be based on a failure to recognise that marrow ischaemia accompanies natural senescence, affecting transcortical haemodynamics, and entraining an increasing periosteal supply for bone survival in old age. The change over from a medullary to a periosteal blood supply to bone cortex is the consequence of medullary ischaemia and reduced marrow arterial pressure, brought about by medullary atherosclerosis.

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